With chronicity, IL-6/STAT3 and TGF-β/SMAD axes remain engaged, Th1/Th17 polarization intensifies alongside inducible regulatory T cells, and myeloid programs skew toward suppression [tumor-associated macrophages (TAMs) and myeloid-derived suppressor cells (MDSCs)] (4). The gene discussed is TGFB1; the disease is neoplasm.